Knockdown of GSG2 inhibits prostate cancer progression in vitro and in vivo

Int J Oncol. 2020 Jul;57(1):139-150. doi: 10.3892/ijo.2020.5043. Epub 2020 Apr 13.

Abstract

Prostate cancer (PCa) is the second leading cause of cancer‑related death among men worldwide. The present study aimed to investigate the role of germ cell‑specific gene 2 protein (GSG2), also termed histone H3 phosphorylated by GSG2 at threonine‑3, in the development and progression of PCa. GSG2 expression levels in PCa tissues and para‑carcinoma tissues was detected by immunohistochemistry. The GSG2 knockdown cell model was constructed by lentivirus infection, and the knockdown efficiency was verified by qPCR and WB. In addition, the effects of shGSG2 on cell proliferation, colony formation and apoptosis were evaluated by Celigo cell counting assay, Giemsa staining and flow cytometry, respectively. Tumor development in nude mice was also detected. GSG2 expression was upregulated in PCa tissues and human PCa cell lines PC‑3 and DU 145. High expression of GSG2 in tumor samples was associated with progressed tumors. GSG2 knockdown suppressed cell proliferation and colony formation, but promoted apoptosis, which was also verified in vivo. The results of the present study revealed that GSG2 upregulation was associated with PCa progression; GSG2 knockdown inhibited cell proliferation and colony formation and induced apoptosis, and may therefore serve as a potential therapeutic target for PCa therapy.

Keywords: GSG2; prostate cancer; proliferation; apoptosis.

MeSH terms

  • Aged
  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Carcinoma / genetics*
  • Carcinoma / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Proliferation / genetics
  • Disease Progression
  • Gene Expression Regulation, Neoplastic*
  • Gene Knockdown Techniques
  • Histones / metabolism
  • Humans
  • Intracellular Signaling Peptides and Proteins / antagonists & inhibitors
  • Intracellular Signaling Peptides and Proteins / genetics
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Male
  • Mice
  • Middle Aged
  • Phosphorylation / genetics
  • Prostate / pathology*
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / pathology
  • Protein Serine-Threonine Kinases / antagonists & inhibitors
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • RNA, Small Interfering / metabolism
  • Up-Regulation / drug effects
  • Xenograft Model Antitumor Assays

Substances

  • Antineoplastic Agents
  • Histones
  • Intracellular Signaling Peptides and Proteins
  • RNA, Small Interfering
  • HASPIN protein, human
  • Protein Serine-Threonine Kinases